title: Cypermethrin exposure during puberty induces oxidative stress and endocrine disruption in male mice.
abstract: Cypermethrin (CYP) is one of the most common contaminants in the ecosystem. The effects of CYP exposure on the induction of oxidative stress and endocrine disruption were studied in adolescent male ICR mice. The hepatic activities of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) and total antioxidant capacity (T-AOC) increased significantly after 3 weeks (postnatal day 21-42) of oral administration of 20 mg kg(-1) CYP. In accordance with the enzyme activities, the mRNA levels for the genes encoding these antioxidant proteins, such as Sod1, Sod2, Gpx1 and Gpx2, were also up-regulated significantly in the 10 and 20 mg kg(-1) CYP treatment groups. Furthermore, we also found that the 3-week oral administration of CYP decreased transcription levels of key genes in pathways of cholesterol synthesis and transport and testosterone synthesis including HMG-CoA synthase, steroidogenic acute regulatory protein (StAR) and cytochrome P450 17α-hydroxysteroid dehydrogenase (P450 17α in the liver and testes. Serum testosterone levels also decreased significantly in mice after treatment with 20 mg kg(-1) CYP. Taken together, the results indicated that CYP can induce endocrine disruption in adolescent mice. The findings will be helpful in elucidating the mechanism of toxicity induced by CYP in adolescent mice.
authors.affiliation: College of Biological and Environmental Engineering, Zhejiang University of Technology, Hangzhou 310032, China.
authors.forename: Yuanxiang
authors.initials: Y
authors.lastname: Jin
authors.forename: Linggang
authors.initials: L
authors.lastname: Wang
authors.forename: Meili
authors.initials: M
authors.lastname: Ruan
authors.forename: Jingwen
authors.initials: J
authors.lastname: Liu
authors.forename: Yuefeng
authors.initials: Y
authors.lastname: Yang
authors.forename: Cheng
authors.initials: C
authors.lastname: Zhou
authors.forename: Bin
authors.initials: B
authors.lastname: Xu
authors.forename: Zhengwei
authors.initials: Z
authors.lastname: Fu
mesh_terms: D000818:Animals; D002374:Catalase / Q000235:genetics / Q000378:metabolism; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D052244:Endocrine Disruptors / Q000633:toxicity*; D004703:Endocrine System / Q000187:drug effects* / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D006904:Hydroxymethylglutaryl-CoA Synthase / Q000235:genetics / Q000378:metabolism; D006913:Hydroxysteroid Dehydrogenases / Q000235:genetics / Q000378:metabolism; D007306:Insecticides / Q000633:toxicity*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018384:Oxidative Stress; D010750:Phosphoproteins / Q000235:genetics / Q000378:metabolism; D011722:Pyrethrins / Q000633:toxicity*; D012333:RNA, Messenger / Q000378:metabolism; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D013737:Testis / Q000187:drug effects / Q000378:metabolism; D000098682:Steroidogenic Acute Regulatory Protein
chemical_list: D052244:Endocrine Disruptors; D007306:Insecticides; D010750:Phosphoproteins; D011722:Pyrethrins; D012333:RNA, Messenger; D000098682:Steroidogenic Acute Regulatory Protein; C017160:cypermethrin; D003577:Cytochrome P-450 Enzyme System; D006913:Hydroxysteroid Dehydrogenases; C035507:3(17)-hydroxysteroid dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D006904:Hydroxymethylglutaryl-CoA Synthase